Page 902 - Veterinary Immunology, 10th Edition
P. 902

macrophages accumulate around the blood vessels of the omentum
  VetBooks.ir  and serosa (Fig. 27.9). These macrophages are activated in that they

               are strongly positive for CD18 and produce TNF-α and IL-1β.
               Endothelial cells upregulate MHC class II expression. These

               antibodies also generate immune-complexes that are deposited in
               the serosa, causing pleuritis or peritonitis, and in glomeruli, leading
               to glomerulonephritis. The serosal vasculitis is responsible for the
               effusion of fibrin-rich fluid into the serosal cavities. This massive

               production of immune-complexes may also be responsible for the
               disseminated intravascular coagulation seen in these cats. IL-1 and
               IL-6 are found in unusually high concentrations in the peritoneal
               fluid from cats with effusive FIP. Cats with preexisting high levels

               of antibodies against FECV develop effusive FIP rapidly on
               challenge. Administering antiserum to FECV before FIP challenge
               may also enhance the peritonitis. It has been suggested that FECV-
               infected cats do not develop FIP since they avoid excessive

               macrophage activation by upregulating IL-10.































                            FIG. 27.9  Granulomatous vasculitis of serosal blood vessels in a
                               cat with feline infectious peritonitis. Note the marked cellular
                            infiltration of the vessel adventitia and media. This lesion may be
                             due to the deposition of virus-antibody complexes in the vessel
                                              walls. (Courtesy Dr. R.C. Weiss.)


                  A modified live intranasal vaccine is available against FIP. The
               vaccine contains a temperature-sensitive mutant virus that
               replicates in the upper respiratory tract and induces a local IgA




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